Resident perspectives on the impact of program leadership communication on well-being during the COVID-19 pandemic.

BACKGROUND: The COVID-19 pandemic introduced a myriad of changes that negatively impacted resident physicians' well-being. Communication from program leadership may mitigate resident stress during times of crisis, yet literature supporting this premise is scant, and best communication practices remain uncertain. This qualitative study aimed to identify stressors to residents and explore the influence of residency program leadership's communication on emotional stress during the COVID-19 pandemic. METHODS: Informed by Kotter's 8-step management model to support resident well-being, this qualitative study used grounded theory methods to interview 25 residents from three training programs (Pediatrics, Internal Medicine, and Medicine-Pediatrics) on a single academic medical campus from May-September 2020. Four investigators coded the data using the constant comparative analysis. Sampling continued until reaching thematic saturation. Codes were built using an iterative approach and organized into themes. Discrepancies were resolved by consensus discussion among investigators. RESULTS: Residents described increased stress levels, the all-consuming nature of COVID-19, mixed emotions about their role as healthcare providers, new coping mechanisms, and changes to their education and work environment that impacted stress. Communication from leadership to residents during the pandemic varied. Effective communication helped mitigate stress; perceived suboptimal communication exacerbated stress. Who was communicating, methods of communication, and content of communication influenced resident stress. CONCLUSIONS: The COVID-19 pandemic introduced new stressors and challenges to residents. The perception of leadership communication played a critical role in mitigating or exacerbating resident stress. We propose a communication framework ("Who? What? Where? When? How?") that residency leadership can utilize during times of crisis.

Antenatal Endotoxin Induces Dysanapsis in Experimental Bronchopulmonary Dysplasia.

Bronchopulmonary dysplasia (BPD), the chronic lung disease of prematurity, is characterized by impaired lung development with sustained functional abnormalities due to alterations of airways and the distal lung. Although clinical studies have shown striking associations between antenatal stress and BPD, little is known about the underlying pathogenetic mechanisms. Whether dysanapsis, the concept of discordant growth of the airways and parenchyma, contributes to late respiratory disease as a result of antenatal stress is unknown. We hypothesized that antenatal endotoxin (ETX) impairs juvenile lung function as a result of altered central airway and distal lung structure, suggesting the presence of dysanapsis in this preclinical BPD model. Fetal rats were exposed to intraamniotic ETX (10 µg) or saline solution (control) 2 days before term. We performed extensive structural and functional evaluation of the proximal airways and distal lung in 2-week-old rats. Distal lung structure was quantified by stereology. Conducting airway diameters were measured using micro-computed tomography. Lung function was assessed during invasive ventilation to quantify baseline mechanics, response to methacholine challenge, and spirometry. ETX-exposed pups exhibited distal lung simplification, decreased alveolar surface area, and decreased parenchyma-airway attachments. ETX-exposed pups exhibited decreased tracheal and second- and third-generation airway diameters. ETX increased respiratory system resistance and decreased lung compliance at baseline. Only Newtonian resistance, specific to large airways, exhibited increased methacholine reactivity in ETX-exposed pups compared with controls. ETX-exposed pups had a decreased ratio of FEV in 0.1 second to FVC and a normal FEV in 0.1 second, paralleling the clinical definition of dysanapsis. Antenatal ETX causes abnormalities of the central airways and distal lung growth, suggesting that dysanapsis contributes to abnormal lung function in juvenile rats.

Neonatal Vitamin D Status Is Associated with the Severity of Brain Injury in Neonatal Hypoxic-Ischemic Encephalopathy: A Pilot Study.

OBJECTIVE: The primary aim of this study was to evaluate the association between 25-hydroxyvitamin D (25OHD) concentration at birth and the short-term outcomes in neonatal hypoxic-ischemic encephalopathy (HIE). Our secondary aim was to evaluate the effect of postnatal vitamin D supplementation on outcomes in the perinatal period after hypoxic injury. STUDY DESIGN: This retrospective cohort study included all infants ≥35 weeks gestation admitted to a regional level IV neonatal intensive care unit and diagnosed with moderate or severe HIE. Spearman correlation coefficients were used to evaluate associations between clinical outcomes including standardized brain magnetic resonance imaging (MRI) scores and either 25OHD concentrations in the first 48 hours of life or total vitamin D supplementation. RESULT: A total of 43 infants met inclusion criteria; 22 had 25OHD concentrations drawn within the first 48 hours. There was a significant inverse association between 25OHD concentration and brain injury on MRI (p = 0.017). There was a trend toward decreased ventilator days in infants receiving higher doses of vitamin D in the first week of life (p = 0.062), but there was no association between vitamin D dosing and MRI injury. CONCLUSION: These results support an association between lower vitamin-D levels and early adverse outcomes in HIE, including radiographic severity of brain injury.